Abstract
Mechanical forces and the activation of the renin-angiotensin system (RAS) may alter the NO/O2•− balance, imparing endothelial nitric oxide (NO) availability. This study investigates the link between RAS and NO/O2•− balance in human aortic endothelial cells (HAEC) exposed to pulsatile stretch with and without ACE inhibitor quinaprilat or angiotensin II type 1 (AT1) receptor antagonist losartan. Pulsatile stretch increased Ang II levels and O2•− production, reducing NO release. RAS blockade with quinaprilat or losartan restored the balance between NO and O2•−. These results provide a molecular basis for understanding the vascular protective effects of ACE inhibition and AT1 receptor antagonism.
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